Buyse Johan, Janssen Sara, Geelissen Sofie, Swennen Quirine, Kaiya Hiroyuki, Darras Veerle M, Dridi Sami
Laboratory of Livestock Physiology, Immunology and Genetics, Department of Biosystems, K.U. Leuven, Kasteelpark Arenberg 30, 3001 Leuven, Belgium.
Peptides. 2009 Jul;30(7):1342-7. doi: 10.1016/j.peptides.2009.04.015. Epub 2009 May 3.
The endogenous ligand for the growth hormone (GH) secretagogue receptor ghrelin is a peptide secreted by the stomach of mammals and stimulates food intake and enhances adiposity. In avian species, ghrelin is mainly produced by the proventriculus but reduces food intake whereas its effect on lipogenesis in different tissues is unknown. We therefore investigated the effects of a single intravenous injection of 2.8 microg (1 nmol per chick) recombinant chicken ghrelin in neonatal broiler chicks. Besides food intake and plasma corticosterone levels, mRNA levels of the key lipogenic enzyme fatty acid synthase (FAS) and its related transcription factors sterol regulatory element binding protein-1 (SREBP-1) and peroxisome proliferator-activated receptor-gamma (PPARgamma) were determined in diencephalon, liver and quadriceps femoris muscle before, and 15, 30, and 60 min after injection. Chicken ghrelin administration induced a significant short-term (<30 min) reduction in food intake and markedly elevated plasma corticosterone levels. In diencephalon, FAS, SREBP-1 and PPARgamma mRNA levels were significantly increased within 15 min after ghrelin injection. These observations suggest that central fatty acid metabolism is involved in the anorectic effects of ghrelin. In contrast, hepatic mRNA levels of FAS and both transcription factors were significantly reduced within 30 min after ghrelin injection. In muscle, FAS and transcription factor gene expression was very low and not affected by ghrelin. Overall, our results indicate that ghrelin has opposite effects on FAS and transcription factor mRNA amounts with increased levels in diencephalon (central anorectic effect) and decreased levels in liver (peripheral anti-lipogenic effect) in chickens.
生长激素促分泌素受体的内源性配体胃饥饿素是一种由哺乳动物胃分泌的肽，可刺激食物摄入并增加肥胖。在鸟类中，胃饥饿素主要由腺胃产生，但会减少食物摄入，而其对不同组织脂肪生成的影响尚不清楚。因此，我们研究了对新生肉鸡单次静脉注射2.8微克（每只雏鸡1纳摩尔）重组鸡胃饥饿素的效果。除了食物摄入量和血浆皮质酮水平外，还在注射前以及注射后15、30和60分钟测定了间脑、肝脏和股四头肌中关键脂肪生成酶脂肪酸合酶（FAS）及其相关转录因子固醇调节元件结合蛋白-1（SREBP-1）和过氧化物酶体增殖物激活受体-γ（PPARγ）的mRNA水平。给予鸡胃饥饿素导致食物摄入量显著短期（<30分钟）减少，并使血浆皮质酮水平明显升高。在间脑中，胃饥饿素注射后15分钟内FAS、SREBP-1和PPARγ的mRNA水平显著增加。这些观察结果表明，中枢脂肪酸代谢参与了胃饥饿素的厌食作用。相比之下，胃饥饿素注射后30分钟内肝脏中FAS和这两种转录因子的mRNA水平显著降低。在肌肉中，FAS和转录因子基因表达非常低，且不受胃饥饿素影响。总体而言，我们的结果表明，胃饥饿素对鸡的FAS和转录因子mRNA量具有相反的影响，在间脑水平升高（中枢厌食作用），在肝脏水平降低（外周抗脂肪生成作用）。
